SARS-CoV-2 uses major endothelial integrin αvβ3 to cause vascular dysregulation in-vitro during COVID-19.
Issue Date
2021-06-23Keywords
COVID-19CORONAVIRUS
cardiovascular complications
Metadata
Show full item recordJournal
PloS oneDOI
10.1371/journal.pone.0253347PubMed ID
34161337Item Type
ArticleLanguage
enEISSN
1932-6203ae974a485f413a2113503eed53cd6c53
10.1371/journal.pone.0253347
Scopus Count
Collections
Related articles
- Molecular Cross-Talk between Integrins and Cadherins Leads to a Loss of Vascular Barrier Integrity during SARS-CoV-2 Infection.
- Authors: Nader D, Kerrigan SW
- Issue date: 2022 Apr 25
- Biological and Clinical Consequences of Integrin Binding via a Rogue RGD Motif in the SARS CoV-2 Spike Protein.
- Authors: Makowski L, Olson-Sidford W, W-Weisel J
- Issue date: 2021 Jan 20
- The integrin antagonist cilengitide activates alphaVbeta3, disrupts VE-cadherin localization at cell junctions and enhances permeability in endothelial cells.
- Authors: Alghisi GC, Ponsonnet L, Rüegg C
- Issue date: 2009
- Coronaviruses and Integrin αvβ3: Does Thyroid Hormone Modify the Relationship?
- Authors: Davis PJ, Lin HY, Hercbergs A, Keating KA, Mousa SA
- Issue date: 2020 Aug
- Endothelial dysfunction in COVID-19: a position paper of the ESC Working Group for Atherosclerosis and Vascular Biology, and the ESC Council of Basic Cardiovascular Science.
- Authors: Evans PC, Rainger GE, Mason JC, Guzik TJ, Osto E, Stamataki Z, Neil D, Hoefer IE, Fragiadaki M, Waltenberger J, Weber C, Bochaton-Piallat ML, Bäck M
- Issue date: 2020 Dec 1